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Primary open angle glaucoma (OAG) is a multi-factorial optic neuropathy characterized by progressive retinal ganglion cell death and associated visual field loss. Glaucoma prevalence is 0.7% among 40-49 year olds and rises over subsequent decades to 7.7% amongst those over 80 years of age.1 Due to the aging of the United States population, the number of patients with OAG is expected to increase by 50% to 3.36 million in the year 2020.2 OAG therefore represents an emerging disease with increasing cost and negative visual function impacts; yet our understanding of OAG risk factors and treatments are not fully apparent. The only treatable risk factor for glaucoma is elevated intraocular pressure (IOP). Despite the medical lowering of IOP, however, some glaucoma patients continue to experience disease progression and subsequent irreversible blindness. For instance, in the early manifest glaucoma trial (EMGT) the disease progression rate in the treatment group was 45% as compared to 62% in the control arm.3 In the collaborative initial glaucoma treatment study (CIGTS) substantial visual field (VF) loss occurred in 10-13.5% of participants during 5 years of followup.4 Specifically, increased incidence of visual field deterioration occurred with older age (increased risk of VF loss by 40% every 10 years), race (nonwhites had a 50% increased risk relative to whites) and diabetes (59% increased risk relative to non-diabetic patients).4 In a similar manner, 20% of normal tension glaucoma (NTG) patients show continued visual field loss even after 5 years of IOP reduction treatment.5 Although IOP is still considered the only OAG risk factor, it is clear that glaucoma is a complex disease that is not prevented or cured by using only IOP reducing therapies in all patients. Among the other OAG risk factors, compromised ocular blood flow and faulty vascular autoregulation continue to emerge as possible contributors to OAG disease pathophysiology. Vascular related OAG risk factors have been found in prospective, retrospective and large epidemiological studies throughout the world. Growing evidence suggests that glaucoma patients have reduced blood flow to the retina, choroid and optic nerve. It is unclear whether there is a primary contributing vascular component that promotes damage to the optic nerve and retinal ganglion cells (as well as aqueous humor dysregulation), if the OAG vascular component is secondary to increased IOP, or if it represents a combination of the two including impaired autoregulation within the OAG population.6 Several of the most common vascular risk factors which may be related to OAG disease include: aging, systemic blood pressure, nocturnal hypotension, ocular perfusion pressure, migraine, disk hemorrhage, diabetes and directly assessed reductions of ocular blood flow. Each of these topics will be reviewed in detail within this manuscript.

Physiology: The Clinical Significance of Vascular Factors in Glaucoma